In Japan, an estimated 1.5-2.0 million people are persistently infected with hepatitis C virus (HCV), and it is assumed that most carriers show the symptoms of chronic hepatitis (see non-patent reference 1). With respect to hepatitis B, there are many cases where the infection does not cause chronic hepatitis, but directly develops liver cancer. By contrast, 80 to 90% of HCV-infected persons develop chronic liver disease based on observations of liver tissue, and there is a possibility that 50 to 60% of HCV-infected persons develop cirrhosis or hepatocellular carcinoma via chronic hepatitis (see non-patent reference 2). HCV infection has become a major clinical problem worldwide.
Interferons (IFNs) are a highly-homologous and species-specific protein family that regulates the immune response by inhibiting viral replication and cell proliferation, and it is known that there are four classes of interferons in humans (non-patent reference 3).
Interferons are applied to various viral diseases on the basis of the antiviral effects thereof. In particular, for the treatment of chronic hepatitis C that is caused by the infection of HCV, a virus having a positive-stranded RNA genome, IFNs are widely used to eliminate HCV. However, it is known that IFNs have low therapeutic effects for patients infected with HCV genotype 1b or having a high viral load (1 Meq or higher) (see non-patent references 4 and 5). This genotype and high viral load are factors that affect the therapeutic effects of IFN, and such patients account for 70% or more of those with chronic hepatitis C in Japan. In addition, side effects such as fever, weakness, and psychiatric disorders are frequently observed.
As conventional treatments for a patient infected with genotype 1b and having a high viral load, a combination therapy of ribavirin with IFN, and a combination therapy of ribavirin with PEG-interferon α-2a (PEG-IFN α-2a) or PEG-interferon α-2b (PEG-IFN α-2b) are known. These therapeutic effects (complete response rate) are not enough. Even the most effective combination therapy of ribavirin with PEG-IFN at present shows a complete response rate of, at most, approximately 50%. Further, compared to a treatment with IFN alone, side effects such as reductions of hemoglobin, erythrocytes, and leukocytes are frequently observed in the IFN/ribavirin therapy. When PEG-IFN α-2a is used, influenza-like symptoms are milder than those caused by IFN, but skin reactions and reductions of lymphocytes, platelets, and erythrocytes are more frequently observed. In the combination therapy of ribavirin with PEG-IFN α-2b, disorders at the injection site frequently occur, recovery of laboratory test values for adverse effects on hematology slows slightly and, in elderly patients, the frequencies of highly abnormal laboratory test values and dose reduction tend to become high. Under these circumstances, the development of treatments effective for a case where sufficient effects are not obtained by IFN treatment, a case where effectiveness by IFN administration is not expected due to genotype 1b or a high viral load, a case of an elderly patient, a case where the infection develops cirrhosis, and the like, is desired.
22β-methoxyolean-12-ene-3β,24(4β)-diol is a compound having the following structure, and is known to have an inhibitory effect on hepatocyte disorder (see patent references 1 and 2).

Further, it was reported that 22β-methoxyolean-12-ene-3β,24(4β)-diol had an anti-HCV effect (see non-patent reference 6), and this compound is expected to be developed as a therapeutic agent for viral liver diseases. However, effects obtained by combining this compound with other drugs have not been studied.    [patent reference 1] International Publication WO97/03088    [patent reference 2] Japanese Patent No. 3279574    [non-patent reference 1] The Japan Society of Hepatology, ed., “Mansei kanen no chiryo gaido (Guidelines of treatment for chronic hepatitis)”, BUNKODO Co., Ltd., 2006, p. 21    [non-patent reference 2] Shiro IINO, “The guideline of treatment for hepatitis C”, Nippon Rinsho, 2004, vol. 62, suppl. 7, p. 342-346    [non-patent reference 3] Annual Review of Biochemistry, U.S.A., 1987, vol. 56, p. 727-777    [non-patent reference 4] Shiro IINO, “Akiraka ni natta interferon no kouka to genkai (Revealed effects and limit of interferon)”, Naika, 1999, vol. 84, no. 2, p. 285-291    [non-patent reference 5] Lancet, United Kingdom, 1998, vol. 352, no. 9138, p. 1426-1432    [non-patent reference 6] Hepatology, U.S.A., 2005, vol. 42, p. 248A